Differential Expression of Extracellular Matrix and Adhesion Molecules in Fetal-Origin Amniotic Epithelial Cells of Preeclamptic Pregnancy

• Published in: PloS one Vol. 11; no. 5; p. e0156038
• Main Authors: Kim, Myung-Sun, Yu, Ji Hea, Lee, Min-Young, Kim, Ah Leum, Jo, Mi Hyun, Kim, MinGi, Cho, Sung-Rae, Kim, Young-Han
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 24.05.2016; Public Library of Science (PLoS)
• Subjects: Adhesion; Adult; Amnion - cytology; Amnion - metabolism; Annotations; Arteries; Arthritis; Biology and Life Sciences; Biomedical research; Brain research; Cell adhesion molecules; Cell Adhesion Molecules - genetics; Cell Adhesion Molecules - metabolism; Cells, Cultured; Cesarean section; Consent; Encyclopedias; Epithelial cells; Epithelial Cells - metabolism; Epithelial Cells - pathology; Extracellular matrix; Extracellular Matrix - genetics; Extracellular Matrix - metabolism; Female; Fetuses; Gene expression; Gene Expression Profiling - methods; Gene Expression Regulation; Gene Regulatory Networks; Genes; Genetic aspects; Genomes; Gynecology; Health aspects; Hospitals; Humans; Hypertension; Maternal effects; Medical research; Medicine; Medicine and Health Sciences; Morbidity; Neonates; Obstetrics; Physiological aspects; Placenta; Polymerase chain reaction; Pre-eclampsia; Pre-Eclampsia - genetics; Pre-Eclampsia - metabolism; Pre-Eclampsia - pathology; Preeclampsia; Pregnancy; Pregnant women; Rehabilitation; Research and analysis methods; Science; Sequence Analysis, RNA - methods; Signal Transduction; Stem cells; Stromelysin 2; Uterus; Womens health; South Korea
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0156038

Preeclampsia is a common disease that can occur during human pregnancy and is a leading cause of both maternal and neonatal morbidity and mortality. Inadequate trophoblast invasion and deficient remodeling of uterine spiral arteries are associated with preeclampsia (PE). The development of this syndrome is thought to be related to multiple factors. Recently, we isolated patient-specific human amniotic epithelial cells (AECs) from the placentas of 3 women with normal pregnancy and 3 with preeclamptic pregnancy. Since the characteristics of human AECs in PE are different from those in normal pregnancy, we sought to confirm the genes differentially expressed between preeclamptic pregnancy and normal pregnancy. Therefore, we performed transcriptome analysis to investigate the candidate genes associated with the possible pathophysiology of preeclampsia. Pathway analysis was performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) and Kyoto Encyclopedia of Genes and Genomes (KEGG) online resource. In this study, we selected a total of 12 pathways and focused on extracellular matrix-related and biological adhesion molecules. Using RT-PCR array and real-time PCR, we confirmed that COL16A1, ITGB2, and LAMA3 were significantly up-regulated, but ITGA1, ITGA3, ITGA6, MMP1, MMP3, MMP10 and MMP11 were significantly down-regulated in preeclamptic fetal origin cells. Taken together, we suggest that the genes and pathways identified here may be responsible for the occurrence and development of PE, and controlling their expression may play a role in communication with fetal-maternal placenta to keep normal pregnancy.